ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

T. C. Yuan, F. F. Lin, S. Veeramani, S. J. Chen, H. S. Earp, M. F. Lin

Research output: Contribution to journalArticlepeer-review

22 Scopus citations

Abstract

Aberrant regulation in the adhesive ability of cancer cells is closely associated with their metastatic activity. In this study, we examine the role of ErbB-2 in regulating the adhesive ability of androgen receptor (AR)-positive human prostate cancer (PCa) cells, the major cell population of PCa. Utilizing different LNCaP and MDA PCa2b cells as model systems, we found that ErbB-2 activity was correlated with PYK2 activity and adhesive ability in those cells. Increased ErbB-2 expression or activity in LNCaP C-33 cells enhanced PYK2 activation and cell adhesion, while the high PYK2 activity and the rapid adhesion of LNCaP C-81 cells were decreased by diminishing ErbB-2 expression or activity. Knockdown studies revealed the predominant role of ErbB-2 in regulating LNCaP C-81 cell adhesion. Coimmunoprecipitation showed that C-81 cells had increased interaction between ErbB-2 and PYK2. Elevated ErbB-2 activity in LNCaP cells correlated with increased ERK/MAPK activity and enhanced adhesive ability, which were abolished by the expression of K457A-PYK2 mutant or the treatment of PD98059, a MEK inhibitor. In summary, our data suggested that ErbB-2, via PYK2-ERK/MAPK, upregulates the adhesive ability of AR-positive human PCa cells.

Original languageEnglish (US)
Pages (from-to)7552-7559
Number of pages8
JournalOncogene
Volume26
Issue number54
DOIs
StatePublished - Nov 29 2007

Keywords

  • Cell adhesion
  • ErbB-2
  • PYK2
  • Prostate cancer

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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